Methods and apparatus for tachycardia rate hysteresis for dual-chamber cardiac stimulators

ABSTRACT

It has been determined that certain dual-chambered cardiac stimulators may operate in a region in which an atrial pacing event may obscure the detection of a ventricular tachyarrhythmia Various exemplary techniques may be used to improve the ability of dual-chamber cardiac stimulators to detect such ventricular events. In accordance with one technique, it is determined whether a ventricular event should be classified as a ventricular tachyarrhythmia. If not, the VA interval is restarted as usual. However, if the ventricular event may be classified as a ventricular tachyarrhythmia, it is determined whether the ventricular event falls within the region in which an atrial pacing event may obscure its detection. If not, then the VA interval is restarted as usual. However, if the ventricular event falls within this region, the VA interval is restarted with the VT rate detection boundary. This has the effect of lengthening the VA interval and the AA interval in this region so that atrial pacing events will not obscure the sensing and treatment of ventricular tachyarrhythmias in the region.

CROSS REFERENCE TO RELATED APPLICATIONS

This application is a division of U.S. patent application Ser. No.09/332,781, filed on Jun. 14, 1999, now issued as U.S. Pat. Ser. No.6,233,485, the specification of which is incorporated herein byreference.

BACKGROUND OF THE INVENTION

1. Field of the Invention

The present invention relates generally to cardiac stimulators and, moreparticularly, to dual-chamber cardiac stimulators that have an improvedability to detect tachyarrhythmias.

2. Description of the Related Art

As most people are aware, the human heart is an organ having fourchambers. A septum divides the heart in half, with each half having twochambers. The upper chambers are referred to as the left and rightatria, and the lower chambers are referred to as the left and rightventricles. Deoxygenated blood enters the right atrium through thepulmonary veins. Contraction of the right atrium and of the rightventricle pump the deoxygenated blood through the pulmonary arteries tothe lungs where the blood is oxygenated. This oxygenated blood iscarried to the left atrium by the pulmonary veins. From this cavity, theoxygenated blood passes to the left ventricle and is pumped to a largeartery, the aorta, which delivers the pure blood to the other portionsof the body through the various branches of the vascular system.

In the normal human heart, the sinus node (generally located near thejunction of the superior vena cava and the right atrium) constitutes theprimary natural pacemaker by which rhyhnic electrical excitation isdeveloped. The cardiac impulse arising from the sinus node istransmitted to the two atrial chambers. In response to this excitation,the atria contract, pumping blood from those chambers into therespective ventricles. The impulse is transmitted to the ventriclesthrough the atrioventricular (AV) node to cause the ventricles tocontract. This action is repeated in a rhythmic cardiac cycle in whichthe atrial and ventricular chambers alternately contract and pump, thenrelax and fill. One-way valves between the atrial and ventricularchambers in the right and left sides of the heart and at the exits ofthe right and left ventricles prevent backflow of the blood as it movesthrough the heart and the circulatory system.

The sinus node is spontaneously rhythmic, and the cardiac rhythmoriginating from the sinus node is referred to as sinus rhythm. Thiscapacity to produce spontaneous cardiac impulses is called rhythmicity.Some other cardiac tissues also possess this electrophysiologic propertyand, hence, constitute secondary natural pacemakers. However, the sinusnode is the primary pacemaker because it has the fastest spontaneousrate and because the secondary pacemakers tend to be inhibited by themore rapid rate at which impulses are generated by the sinus node.

The resting rates at which sinus rhythm occurs in normal people differfrom age group to age group, generally ranging between 110 and 150 beatsper minute (“bpm”) at birth, and gradually slowing in childhood to therange between 65 and 85 bpm usually found in adults. The resting sinusrate, typically referred to simply as the “sinus rate,” varies from oneperson to another and, despite the aforementioned usual adult range, isgenerally considered to lie anywhere between 60 and 100 bpm (the “sinusrate range”) for the adult population.

A number of factors may affect the sinus rate, and some of those factorsmay slow or accelerate the rate sufficiently to take it outside of thesinus rate range. Slow rates (below 60 bpm) are referred to as sinusbradycardia, and high rates (above 100 bpm) are referred to as sinustachycardia. In particular, sinus tachycardia observed in healthy peoplearises from various factors which may include physical or emotionalstress, such as exercise or excitement, consumption of beveragescontaining alcohol or caffeine, cigarette smoking, and the ingestion ofcertain drugs. The sinus tachycardia rate usually ranges between 101 and160 bpm in adults, but has been observed at rates up to (and ininfrequent instances, exceeding) 200 bpm in younger persons duringstrenuous exercise.

Sinus tachycardia is sometimes categorized as a cardiac arrhythmia,since it is a variation from the normal sinus rate range. Arrhythmiarates which exceed the upper end of the sinus rate range are termedtachyarrhythmias. Healthy people usually experience a gradual return totheir normal sinus rate after the removal of the factors giving rise tosinus tachycardia. However, people suffering from disease may experienceabnormal arrhythmias that may require special, and in some instancesimmediate, treatment. In this text, we typically refer to abnormallyhigh rates that have not yet been determined to be caused by myocardialmalfunction as tachycardias and to abnormally high rates that have beendetermined to be caused by myocardial malfunction as tachyarrhythmias.

It should also be appreciated that an abnormal tachyarrhythmias mayinitiate fibrillation. Fibrillation is a tachyarrhythmia characterizedby the commencement of completely uncoordinated random contractions bysections of conductive cardiac tissue of the affected chamber, quicklyresulting in a complete loss of synchronous contraction of the overallmass of tissue and a consequent loss of the blood-pumping capability ofthat chamber.

In addition to rhythmicity, other electrophysiologic properties of theheart include excitability and conductivity. Excitability, which is theproperty of cardiac tissue to respond to a stimulus, varies with thedifferent periods of the cardiac cycle. As one example, the cardiactissue is not able to respond to a stimulus during the absoluterefractory phase of the refractory period, which is approximately theinterval of contraction from the start of the QRS complex to thecommencement of the T wave of the electrocardiogram. As another example,the cardiac tissue exhibits a lower than usual response during anotherportion of the refractory period constituting the initial part of therelative refractory phase, which is coincident with the T wave. Also,the excitability of the various portions of the cardiac tissue differsaccording to the degree of refractoriness of the tissue.

Similarly, the different portions of the heart vary significantly inconductivity, which is a related electrophysiologic property of cardiactissue that determines the speed with which cardiac impulses aretransmitted. For example, ventricular tissue and atrial tissue are moreconductive than AV junction tissue. The longer refractory phase andslower conductivity of the AV junction tissue give it a significantnatural protective function, as described in more detail later.

For a variety of reasons, a person's heart may not function properlyand, thus, endanger the person's well-being. Most typically, heartdisease affects the rhythmicity of the organ, but it may also affect theexcitability and/or conductivity of the cardiac tissue as well. As mostpeople are aware, medical devices have been developed to facilitateheart function in such situations. For instance, if a person's heartdoes not beat properly, a cardiac stimulator may be used to providerelief. A cardiac stimulator is a medical device that deliverselectrical stimulation to a patient's heart. A cardiac stimulatorgenerally includes a pulse generator for creating electrical stimulationpulses and a conductive lead for delivering these electrical stimulationpulses to the designated portion of the heart. As described in moredetail below, cardiac stimulators generally supply electrical pulses tothe heart to keep the heart beating at a desired rate, although they maysupply a relatively larger electrical pulse to the heart to help theheart recover from fibrillation.

Early pacemakers were devised to treat bradycardia. These pacemakers didnot monitor the condition of the heart. Rather, early pacemakers simplyprovided stimulation pulses at a fixed rate and, thus, kept the heartbeating at that fixed rate. However, it was found that pacemakers ofthis type used an inordinate amount of energy due to the constant pulseproduction. Even the sinus node of a heart in need of a pacemaker oftenprovides suitable rhythmic stimulation occasionally. Accordingly, if aheart, even for a short period, is able to beat on its own, providing anelectrical stimulation pulse using a pacemaker wastes the pacemaker'senergy.

To address this problem, pacemakers were subsequently designed tomonitor the heart and to provide stimulation pulses only when necessary.These pacemakers were referred to as “demand” pacemakers because theyprovided stimulation only when the heart demanded stimulation. If ademand pacemaker detected a natural heartbeat within a prescribed periodof time, typically referred to as the “escape interval”, the pacemakerprovided no stimulation pulse. Because monitoring uses much less powerthan generating stimulation pulses, the demand pacemakers took a largestep toward conserving the limited energy contained in the pacemaker'sbattery.

Clearly, the evolution of the pacemaker did not cease with the advent ofmonitoring capability. Indeed, the complexity of pacemakers hascontinued to increase in order to address the physiological needs ofpatients as well as the efficiency, longevity, and reliability of thepacemaker. For instance, even the early demand pacemakers providedstimulation pulses, when needed, at a fixed rate, such as 70 pulses perminute. To provide a more physiological response, pacemakers having aprogrammably selectable rate were developed. So long as the heart wasbeating above this programmably selected rate, the pacemaker did notprovide any stimulation pulses. However, if the heart rate fell belowthis programmably selected rate, the pacemaker sensed the condition andprovided stimulation pulses as appropriate.

Another major step in adding complexity and functionality to pacemakersoccurred with the advent of pacemakers that had dual chamber capability.Dual chamber pacemakers are capable of sensing and/or pacing in twochambers, typically the right atrium and right ventricle. Accordingly,the distal ends of an atrial lead and a ventricular lead are coupled tothe dual chamber pacemaker. The proximal end of the atrial lead isthreaded through the pulmonary vein and into the right atrium of theheart. Similarly, the proximal end of the ventricular lead is threadedthrough the pulmonary vein, through the right atrium, and into the rightventricle of the heart. Each lead includes a mechanism on its proximalend that attaches to the inner wall of the heart to establish therequired electrical connection between the pacemaker and the heart. Dualchamber pacemakers, as compared to single chamber pacemakers, typicallyfunction in a more physiologically correct manner.

To provide even further physiological accuracy, pacemakers have now beendeveloped that automatically change the rate at which the pacemakerprovides stimulation pulses. These pacemakers are commonly referred toas “rate-responsive” pacemakers. Rate-responsive pacemakers sense aphysiological parameter of the patient and alter the rate at which thestimulation pulses are provided to the heart. Typically, this monitoredphysiological parameter relates to the changing physiological needs ofthe patient. For instance, when a person is at rest, the person's heartneed only beat relatively slowly to accommodate the person'sphysiological needs. Conversely, when a person is exercising, theperson's heart tends to beat rather quickly to accommodate the person'sheightened physiological needs.

Unfortunately, the heart of a person in need of a pacemaker may not beable to beat faster on its own. Prior to the development ofrate-responsive pacemakers, patients were typically advised to avoidundue exercise, and pacemaker patients that engaged in exercise tendedto tire quickly. Rate-responsive pacemakers help relieve this constraintby sensing one or more physiological parameters of a patient thatindicates whether the heart should be beating slower or faster. If thepacemaker determines that the heart should be beating faster, thepacemaker adjusts its base rate upward to provide a faster pacing rateif the patient's heart is unable to beat faster on its own. Similarly,if the pacemaker determines that the patient's heart should be beatingmore slowly, the pacemaker adjusts its base rate downward to conserveenergy and to conform the patient's heartbeat with the patient's lessactive state.

As noted above, pacemakers have historically been employed primarily forthe treatment of heart rates which are unusually slow, i.e.,bradyarrhythmias. However, over the past several years cardiac pacinghas found significantly increasing usage in the management of heartrates which are unusually fast, i.e., tachyarrhythmias.Anti-tachyarrhythmia pacemakers take advantage of the previouslymentioned inhibitory mechanism that acts on the secondary naturalpacemakers to prevent their spontaneous rhymicity, sometimes termed“postdrive inhibition” or “overdrive inhibition”. In essence, the heartmay be stimulated with a faster than normal pacing rate (1) to suppresspremature atrial or ventricular contractions that might otherwiseinitiate ventricular tachycardia, flutter (a tachyarrhythmia exceeding200 bpm), or fibrillation or (2) to terminate an existingtachyarrhythmia.

Typically, these pulses need only be of sufficient magnitude tostimulate the excitable myocardial tissue in the immediate vicinity ofthe pacing electrode. However, another technique for terminatingtachyarrhythmias, referred to as cardioversion, utilizes apparatus toshock the heart synchronized to the tachyarrhythmia with one or morecurrent or voltage pulses of considerably higher energy content thanthat of the pacing pulses. Defibrillation, a related technique, alsoinvolves applying one or more high energy “countershocks” to the heartin an effort to overwhelm the chaotic contractions of individual tissuesections to allow reestablishment of an organized spreading of actionpotential from cell to cell of the myocardium and, thus, restore thesynchronized contraction of the mass of tissue.

In the great majority of cases, atrial fibrillation is hemodynamicallytolerated and not life-threatening because the atria provide only arelatively small portion (typically on the order of 15 to 20 percent) ofthe total volume of blood pumped by the heart per unit time, typicallyreferred to as cardiac output. During atrial fibrillation, the atrialtissue remains healthy because it is continuing to receive a freshsupply of oxygenated blood as a result of the continued pumping actionof the ventricles. Atrial tachyarrhythmia may also be hemodynamicallytolerated because of the natural protective property of the junctionaltissue attributable to its longer refractory period and slowerconductivity than atrial tissue. This property renders the junctionaltissue unable to respond fully to the more rapid atrial contractions. Asa result, the ventricle may miss every other, or perhaps two of everythree, contractions in the high rate atrial sequence, resulting in 2:1or 3:1 A-V conduction and, thus, maintain relatively strong cardiacoutput and an almost normal rhythm.

Nevertheless, in cases where the patient is symptomatic or at high riskin events of atrial tachyarrhythmia or fibrillation, special treatmentof these atrial disorders may be appropriate. Such circumstances mayinclude, for example, instances where the patient suffers fromventricular heart disease and cannot easily withstand even the smallconsequent reduction of ventricular pumping capability, as well asinstances where the rapid atrial rhythm is responsible for anexcessively rapid ventricular rate. The methods of treatment commonlyprescribed by physicians for treating atrial tachyarrhythmia andfibrillation include medication, catheter ablation, pacing therapy,cardiac shock therapy, and in some cases, surgically creating an A-Vblock and implanting a ventricular pacemaker.

In contrast to the atrial arrhythmias discussed above, cardiac outputmay be considerably diminished during an episode of ventriculartachyarrhythmia because the main pumping chambers of the heart, theventricles, are only partially filled between the rapid contractions ofthose chambers. Moreover, ventricular tachyarrhythmia can present a riskof acceleration of the arrhythmia into ventricular fibrillation. As inthe case atrial fibrillation, ventricular fibrillation is characterizedby rapid, chaotic electrical and mechanical activity of the excitablemyocardial tissue. However, in contrast to atrial fibrillation,ventricular fibrillation manifests an instantaneous cessation of cardiacoutput as the result of the ineffectual quivering of the ventricles—acondition that typically requires almost immediate treatment.

Conventional cardiac stimulators monitor the ventricular rate todetermine the nature of an arrhythmia. When a ventriculartachyarrhythmia is detected, the cardiac stimulator deliversanti-tachyarrhythmia pacing therapy to the ventricle or a higher levelshock to the ventricle.

More recently, there has been a combination of certain complementarytechnologies, namely the combination of anti-tachycardia pacemakers withdual-chamber rate-responsive pacemakers. Generally speaking, adual-chamber rate-responsive anti-tachycardia pacemaker offers improvedperformance over the pacemakers discussed above. However, pacemakers ofthis type exhibit certain disadvantages which are described below alongwith certain exemplary methods and apparatus directed to addressingthese disadvantages.

SUMMARY OF THE INVENTION

Certain aspects commensurate in scope with the disclosed embodiments areset forth below. It should be understood that these aspects arepresented merely to provide the reader with a brief summary of certainforms the invention might take and that these aspects are not intendedto limit the scope of the invention. Indeed, the invention may encompassa variety of aspects that may not be set forth below.

During the operation of a cardiac stimulator, it is generally desirablethat the pacing not delay the detection of a tachyarrhythmia Inconventional cardiac stimulators, such as some of those described above,this function is accomplished by providing discreet rate zones fortachyarrhythmia detection and bradyarrhythmia treatment, where thefastest demand pacing rate is less than the slowest tachyarrhythmiadetection rate. As a result, the shortest pacing interval will always belonger than the longest tachyarrhythmia interval. Thus, this ensuresthat a detected ventricular event will not be followed by a demand pace,which may obscure a tachyarrhythmia event, until the longest possibleinterval for tachyarrhythmia detection has expired. While thisfunctionality works well for cardiac stimulators which pace in theventricle only, it has been discovered that such functionality couldobscure certain tachyarrhythmia events in dual-chambered cardiacstimulators, primarily because the atrial pacing may also obscure thedetection of tachyarrhythmia events.

As described in detail below with respect to the disclosed embodiments,in a conventional dual-chambered cardiac stimulator using suchconventional functionality, there is a region where a ventriculartachyarrhythmia may exceed the tachyarrhythmia detection rate boundaryin a region where the VA interval is shorter than the VT interval. Thus,detection of the ventricular tachyarrhythmia in this region causes theVA interval to be restarted so that an atrial demand pace would bedelivered at the end of the VA interval. Therefore, there is apossibility that this atrial demand pace will obscure the subsequentventricular tachyarrhythmia sensing and, thus, potentially delaydetection of a ventricular tachyarrhythmia.

To address this situation, a number of techniques are described indetail below. In accordance with one technique, it is determined whethera ventricular event should be classified as a ventriculartachyarrhythmia. If not, the VA interval is restarted as usual. However,if the ventricular event may be classified as a ventriculartachyarrhythmia, it is determined whether the ventricular event fallswithin the region in which an atrial pacing event may obscure itsdetection. If not, then the VA interval is restarted as usual. However,if the ventricular event falls within this region, the VA interval isrestarted with the VT rate detection boundary. This has the effect oflengthening the VA interval and the AA interval in this region so thatatrial pacing events will not obscure the sensing and treatment ofventricular tachyarrhythmias in the region.

This technique may be modified by using a tachycardia rate differentthan the ventricular tachycardia rate detection boundary. For example, atachycardia rate may be selected between well tolerated tachyarrhythmiasand moderately tolerated tachyarrhythmias so that the VA interval andthe AA interval are lengthened only when ventricular events fall withinan upper portion of the previously discussed region. Although the welltolerated ventricular tachyarrhythmias may be obscured by atrial pacingevents using this technique, the more clinically significanttachyarrhythmias will not be obscured.

In another modification of the previously discussed technique, it isdetermined whether a ventricular event should be classified as aventricular tachyarrhytia If not, the VA interval is restarted as usual.However, if the ventricular event may be classified as a ventriculartachyarrhythmia, the VA interval is restarted with the VT rate detectionboundary, and the VA interval is extended so that the AA interval doesnot exceed the maximum pacing rate. This technique has the effect oflengthening the AA interval, and thus lowering the pacing rate, only tothe extent required to prevent an atrial pacing event from obscuring aventricular tachyarrhythmia.

Finally, the programmable ranges of various parameters may be restrictedto reduce or eliminate the circumstance in which an atrial pacing eventmay obscure a ventricular tachyarrhythmia. For instance, the VT ratedetection boundary may be set higher than the VA interval so thatventricular events classified as ventricular tachyarrhythmias are alwaysfaster Man the VA interval. Also, the maximum pacing rate may be reducedso that the resulting VA interval is raised above the VT interval in theregion above the VT rate detection boundary. Further, the AV intervalmay be reduced in the region to effectively raise the VA interval abovethe VT interval in the region above the VT rate detection boundary.Indeed, various combinations of these three restriction techniques maybe used to program the cardiac stimulator to best fit a particularpatient's needs while minimizing the region in which ventriculartachyarrhythmias may be obscured by an atrial pacing event.

BRIEF DESCRIPTION OF THE DRAWINGS

The foregoing and other advantages of the invention will become apparentupon reading the following detailed description and upon reference tothe drawings in which:

FIG. 1 illustrates a cardiac stimulator having two leads coupled to apatient's heart;

FIG. 2 illustrates a block diagram of an exemplary cardiac stimulator;

FIG. 3 illustrates a diagram of a typical heart rate spectrum thatillustrates programmable rates at the boundaries of each arrhythmiaclass;

FIG. 4 illustrates a timing diagram of exemplary atrial and ventricularevents;

FIG. 5 illustrates a graphical representation of basic time intervalsversus rate occurring within a conventional dual-chamber cardiacstimulator;

FIG. 6 illustrates a graphical representation of basic time intervalsversus rate for a dual-chamber cardiac stimulator in accordance with thepresent invention;

FIG. 7 illustrates a flow chart depicting the functioning of adual-chamber cardiac stimulator in accordance with FIG. 6;

FIG. 8 illustrates a graphical representation of basic time intervalsversus rate for an alternate embodiment of FIG. 7;

FIG. 9 illustrates a graphical representation of basic time intervalsversus rate for an alternate embodiment of a dual-chamber cardiacstimulator in accordance with the present invention;

FIG. 10 illustrates a flow chart depicting the functioning of a cardiacstimulator in accordance with FIG. 9;

FIG. 11 illustrates a graphical representation of basic time intervalsversus rate for an alternate embodiment of a dual-chamber cardiacstimulator in accordance with the present invention, where the VTboundary rate is set higher than the intersection of the VT and VAcurves;

FIG. 12 illustrates a graphical representation of basic time intervalsversus rate for an alternate embodiment of a dual-chamber cardiacstimulator, where the maximum pacing rate is set low enough so that theresulting VA curve is raised above the VT curve in the region above theVT boundary; and

FIG. 13 illustrates a graphical representation of basic time intervalsversus rate for an alternate embodiment of a dual-chamber cardiacstimulator in accordance with the present invention, where the intervalis reduced so that the resulting VA curve is raised above the VT curvein the region above the VT boundary.

DETAILED DESCRIPTION OF SPECIFIC EMBODIMENTS

Turning now to the drawings, and referring initially to FIG. 1, oneembodiment of a dual-chamber cardiac stimulator is illustrated andgenerally designated by the reference numeral 10. As discussed below,the cardiac stimulator 10 may include an apparatus for adjusting basictime intervals versus rate to enhance the ability of the cardiacstimulator 10 to detect tachyarrhythmias. The general structure andoperation of the cardiac stimulator 10 will be discussed with respect toFIGS. 1-3. Then, the functioning of a conventional dual-chamber cardiacstimulator will be discussed with regard to FIGS. 4 and 5 in order tohighlight certain circumstances that may mask or delay tachyarrhythmiadetection. Once these circumstances have been described, variousexemplary methods for addressing these circumstances will be describedwith reference to FIGS. 6-13.

As shown in FIG. 1, the body of the cardiac stimulator 10 includes acase 12 and a header 14. The cardiac stimulator 10 may be implantable ornon-implantable. If implantable, the case 12 and the header 14 arehermetically sealed to prevent bodily fluids from damaging the internalcircuitry of the cardiac stimulator 10. Typically, the case 12 is madeof titanium, and the header 14 is made of polyethylene.

In the described embodiment, the cardiac stimulator 10 is a dual chambercardioverter/defibrillator (ICD), although it should be understood thatthe teachings set forth herein may apply to other types of cardiacstimulators. Because the cardiac stimulator 10 is a dual chamber ICD, itincludes an atrial lead 16 and a ventricular lead 18. Typically, theleads 16 and 18 are generally flexible and include an electricallyconductive core surrounded by a protective sheath. For instance, theinternal core may be a coiled copper wire, and the protective sheath maybe a coating of polyethylene.

Each lead 16 and 18 includes a respective tip 20 and 22 that is designedto be implanted or coupled to an interior surface of a chamber of theheart 24. As illustrated, the tip 20 of the atrial lead 16 is implantedin an inner wall of the right atrium 26 of the heart 24 for sensingand/or stimulating the right atrium 26. Similarly, the tip 22 of theventricular lead 18 is implanted in an inner wall of the right ventricle28 of the heart 24 for sensing and/or stimulating the right ventricle28.

The cardiac stimulator 10 uses electronic circuitry to perform itsfunctions, such as the circuitry illustrated in FIG. 2 and generallydesignated by the reference numeral 30. A microprocessor 32 providespacemaker control and computational facilities. Although it will beappreciated that other forms of circuitry, such as analog or discretedigital circuitry, can be used in place of microprocessor 32, amicroprocessor is typically advantageous due to its miniature size andits flexibility. A particularly energy efficient microprocessor, whichis designed specifically for use in pacemakers, is fully described inU.S. Pat. Nos. 4,390,022 and 4,404,972, which are assigned to theassignee of my invention.

The microprocessor 32 has input/output ports connected in a conventionalmanner via bidirectional bus 34 to memory 36, an AV interval timer 38,and a pacing interval timer 40. In addition, the AV interval timer 38and pacing interval timer 40 each has an output connected to acorresponding input port of the microprocessor 32 by lines 42 and 44respectively. Memory 36 may include both ROM and RAM, and themicroprocessor 32 may also contain additional ROM and RAM. The pacemakeroperating routine is typically stored in ROM, while the RAM storesprogrammable parameters and variables in conjunction with the pacemakeroperation.

The AV and pacing interval timers 38 and 40 may be external to themicroprocessor 32, as illustrated, or internal thereto. The timers 38and 40 may be, for instance, suitable conventional up/down counters ofthe type that are initially loaded with a count value and count up to ordown from the value and output a rollover bit upon completing theprogrammed count. The initial count value is loaded into the timers 38,40 on bus 34 and the respective rollover bits are output to themicroprocessor 32 on lines 42 and 44.

The microprocessor 32 typically also has an input/output port connectedto a telemetry interface 46 by line 48. The pacemaker, when implanted,is thus able to receive pacing and rate control parameters from anexternal programmer 35 and to send data to an external receiver ifdesired. Many suitable telemetry systems are known to those skilled inthe art. One such system and encoding arrangement is described in U.S.Pat. No. 4,539,992, which is also assigned to the assignee of myinvention.

The microprocessor output ports are connected to inputs of an atrialstimulus pulse generator 50 and a ventricular stimulus pulse generator52 by control lines 54 and 56, respectively. The microprocessor 32transmits pulse parameter data, such as amplitude and width, as well asenable/disable and pulse initiation codes to the generators 50, 52 onthe respective control lines. The microprocessor 32 also has input portsconnected to outputs of an atrial sense amplifier 58 and a ventricularsense amplifier 60 by lines 62 and 64 respectively. The atrial andventricular sense amplifiers 58, 60 detect occurrences of P-waves andR-waves respectively.

The input of the atrial sense amplifier 58 and the output of the atrialstimulus pulse generator 50 are connected to a first conductor 66 whichis inserted in a first conventional lead 68. Lead 68 is inserted into aheart 70 intravenously or in any other suitable manner. The lead 66 hasan electrically conductive pacing/sensing tip 72 at its distal end whichis electrically connected to the conductor 66. The pacing/sensing tip 72is typically lodged in the right atrium 74.

The input of the ventricular sense amplifier 60 and the output of theventricular stimulus pulse generator 52 are connected to a secondconductor 76. The second conductor 76 is inserted in a secondconventional lead 78 which is inserted intravenously or otherwise in theright ventricle 80 of the heart 70. The second lead 78 has anelectrically conductive pacing/sensing tip 82 at its distal end. Thepacing/sensing tip 82 is electrically connected to the conductor 76. Thepacing/sensing tip 82 is typically lodged on the wall of the rightventricle.

The conductors 50, and 52 conduct the stimulus pulses generated by theatrial and ventricular stimulus pulse generators 66, 76, respectively,to the pacing/sensing tips 72, 82. The pacing/sensing tips 72, 82 andcorresponding conductors 66, 76 also conduct sensed cardiac electricalsignals in the right atrium and right ventricle to the atrial andventricular sense amplifiers 58, 60.

In addition, it may be desired to provide defibrillation capability inthe cardiac stimulator 10. if this is the case, a high voltagedefibrillator circuit 84 is provided which is controlled by themicroprocessor 32. The defibrillator circuit 84 is connected to hearttissue through two high voltage leads 86, 88 which communicate with theheart through electrodes 90, 92. In the illustrated embodiment,epicardial patch electrodes are diagrammatically represented. However,other electrode configurations, including endocardial electrodes, mayalso be suitable.

The atrial and ventricular sense amplifiers 58, 60 communicate both withthe microprocessor and with a compressed signal A-to-D converter 94. Thecompressed signal A-to-D converter 94 communicates through the bus 34with memory 36 and the microprocessor 32, primarily, and on a line 96with the telemetry 46. Thus, the output of the converter 94 can bemanipulated by the microprocessor 32, or stored in memory 36 or directlycommunicated through the telemetry 46 to the programmer 35. The storedoutput of the convertor 94 may also be subsequently communicated frommemory 36 through the telemetry 46 to the program 35.

The microprocessor 32 may also base its control on other parameters,such as information received from other sensors. For example, anactivity sensor 98, such as an implanted accelerometer, may be used togather information relating to changing environmental or physiologicalconditions. Although the use of an accelerometer as the activity sensor98 may be advantageous, other types of sensors may also be used to gaugecertain types of physical activity or physical condition, such asvibration sensors, temperature sensors, oxygen sensors, pH sensors,and/or impedance sensors. Indeed, when the dual-chamber cardiacstimulator 10 is operating in rate-responsive mode, the stimulator 10typically adjusts the pacing rate in response to one or more detectedphysiological or environmental parameters conrelated to a physiologicneed.

The operation of the cardiac stimulator 10 may be affected by heartrate. With reference now to FIG. 3, a heart rate spectrum may be storedin the circuitry 30 and partitioned into a multiplicity of regionsdefining contiguous, successive heart rate ranges. At the lower end ofthe illustrated heart rate spectrum is normal rhythm, which isdesignated SINUS. As the heart rate rises along the spectrum, thespectrum enters progressively higher rate ranges associated withventricular tachycardia or tachyarrhythmia, respectively labeled TACH-1,TACH-2, and TACH-3. Beyond the ventricular tachycardia ranges of thespectrum lies the range associated with ventricular fibrillation, whichis labeled FIB.

It will be observed that the spectrum may be partitioned such that therate ranges are representative of respective degrees of hemodynamictolerance of the patient to cardiac rates in those regions. Generallyspeaking, heart rates in the SINUS region are normal, whereas rates inthe FIB region cannot be tolerated. Furthermore, the ascending order ofthe three illustrated ventricular tachyarrhythmia regions TACH-1,TACH-2, and TACH-3 depicts well tolerated, moderately tolerated, andpoorly tolerated classes of tachycardia, respectively. Although treetachyarrhythmia classes are illustrated, the actual number of suchclasses may be greater or fewer depending on the judgment of thephysician regarding the management of anthymias and the prescription oftherapy regimens for a particular patient. As will become clear from thediscussion of therapy considerations below, the number oftachyarrhythmia classes is of less concern than the relationship betweenthe maximum pacing rate and the tachyarrhythmia detection rate boundary.In the examples discussed below, it will be assumed that the end of theSINUS range represents the maximum pacing rate of the cardiac stimulator10 and that the beginning of the TACH-1 range represents the detectionrate boundary for ventricular tachyarrhythmias.

As illustrated in FIG. 4, the pacing rate is determined by the timeinterval between an atrial pace or sensed P-wave A_(p1) until asuccessive atrial pace event A_(p2). Thus, the pace interval AA, whichis illustrated in FIG. 5 as curve 100, essentially defines the pacingrate of the cardiac stimulator 10. After the first atrial pace eventA_(p1), a ventricular pace event V_(p1) occurs. The time intervalbetween the atrial pace event A_(p1) and the ventricular pace eventV_(p1) is defined as the AV interval, which is illustrated in FIG. 5 ascurve 102. After the ventricular pace event V_(p1) a time interval VAextends from the ventricular pace event V_(p1) to the next atrial paceevent A_(p2). The curve 104 of FIG. 5 illustrates an example of a VAinterval. It should be noted that the AV interval when combined with theVA interval equals the AA interval, e.g., the pacing rate.

Referring to FIG. 5, it should be noted that the AV interval curve 102is an adaptive function used in dual-chamber cardiac stimulators, wherethe AV interval decreases from its programmed value, e.g., 200milliseconds, when the atrial rate exceeds a threshold, e.g., 60 BPM,with a decrease of 1 millisecond for every 8 milliseconds decrease inatrial rate. Of course, the AV interval curve 102 could also beillustrated as a constant value. It should also be noted that the AAinterval curve 100 is, as mentioned above, the sum of the AV intervaland the VA interval, although it should be further understood that theVA interval is typically adjusted by the cardiac stimulator to maintainthe desired AA interval based upon changes in the AV interval.

As shown by the AA interval curve 100, the cardiac stimulator in thisexample begins delivering pacing pulses at about 65 BPM. Because thecardiac stimulator is rate responsive, the pacing rate may continue toincrease until it reaches a maximum pacing rate, which is illustrated atpoint 106 as about 140 BPM in this example. Since ventriculartachycardia (VT) detection zones are generally restricted to be abovethe MPR, as discussed previously, a VT interval-versus-rate curve 108 isillustrated to begin at about 150 BPM in this example.

From FIG. 5 it can be seen that if a ventricular tachycardia exceeds thedetection rate boundary of 150 BPM, there is a region where the VTinterval curve 108 exceeds the VA interval curve 104 and forms, in thisexample, a triangle 110 between 150 BPM and approximately 190 BPM. Inthis region, if a ventricular tachycardia R-wave were sensed, the VAinterval would be restarted and an atrial demand pace would be deliveredat the end of the VA interval. However, since the VA interval in thisregion was shorter than the VT interval, the ventricular tachycardia mayoccur during the AV interval. In this situation, the atrial demand paceA_(p) may obscure the ventricular tachycardia R-wave and, thus,potentially delay detection of the ventricular tachycardia. Furthermore,if the atrial pace A_(p) is followed by a ventricular pace V_(p)(because the ventricular tachycardia R-wave was obscured), theventricular pace may occur in a physiologically vulnerable period. Ofcourse, if the ventricular tachycardia exceeds the rate of 190 BPM, theVT interval is less than the VA interval, so the next ventriculartachycardia event would be sensed prior to the next atrial pace A_(p).

In view of the above discussion of FIG. 5, it would be desirable toimprove the ability of a dual-chamber cardiac stimulator to detecttachyarrhythmias, particularly tachyarrhythmias that are at or onlymarginally above the detection rate boundary. One technique foraddressing this problem is described in reference to FIGS. 6 and 7.These figures describe a technique that adds “tachycardia hysteresis” tothe atrial pacing rate to prevent obscuring ventricular tachyarrhytmiasunder atrial pacing.

To carry forward the example illustrated in FIG. 5, it should be notedthat identical or similar reference numerals and the same MPR andtachycardia rate detection boundary are used in FIG. 6. In particular,it should be noted that the AV interval curve 102 and the VT intervalcurve 108 are the same in this example as in the example illustrated inFIG. 5. However, it should be noted that the VA interval curve 104A isskewed upwardly at about the VT rate detection boundary of 150 BPM, asillustrated by the point 105. Indeed, as illustrated by the VA intervalcurve 104A in FIG. 6, the VA interval is lengthened at about the VT ratedetection boundary to make it equal to or greater than the longest VTinterval illustrated by the VT interval curve 108. Due to the additiveeffects of the AV interval curve 102 and the VA interval curve 104A,this action effectively increases the AA interval at point 107, and thusreduces the atrial pacing rate, slightly in the presence of high rateventricular activity. Thus, it should be noted that the AA intervalcurve 100A skews upwardly in a manner similar to that of the VA intervalcurve 104A. It should also be noted that this action removes thetriangle 110. Once the ventricular activity rises above about 190 BPM,the VA curve 104A and the AA curve 100A drop back to previous levels atpoints 109 and 111, respectively.

Referring additionally to FIG. 7, when any ventricular event is detectedat or above the VT rate detection boundary, the VA interval is restartedwith the larger of the VT boundary interval or the operational VA delay.The operational VA delay is defined as the desired AA interval minus theactual proceeding AV interval. In a specific example illustrated in theflow chart 120, when a ventricular event at or above the VT ratedetection boundary is detected, the operational VA delay is computed.(Block 122). It is then determined whether the time from the lastventricular event, i.e., the VV interval, is less than or equal to theVT boundary interval. (Block 124). If the VV interval is less than orequal to the VT rate detection boundary, the detected ventricular eventis not a ventricular tachycardia Therefore, the cardiac stimulatorcontinues to operate in the region of the graph to the left of the MPR106. Accordingly, the VA interval is restarted with the operational VAdelay as illustrated in both FIGS. 5 and 6. (Block 126).

However, if the VV interval is greater than the VT rate detectionboundary, then the ventricular event is indicative of a ventriculartachyarrhythmia. Thus, the cardiac stimulator begins to operate in theregion of the graph of FIG. 6 to the right of the MPR 106. To determinehow to restart the VA interval, it is next determined whether theoperational VA delay is less than the VT rate detection boundary. (Block128). If not, then the VT interval is less than the VA interval so thatthe ventricular event essentially falls within the portion of the graphillustrated in FIG. 5 to the right of the triangle 110. Because, in thisregion, another ventricular event will appear before an atrial pace canbe delivered, the VA interval may be restarted with the operational VAdelay. (Block 126). Thus, the cardiac stimulator 10 operates to theright of the points 109 and 111 illustrated in FIG. 6.

On the other hand, if the operational VA delay is less than the VT ratedetection boundary, the ventricular event falls within the triangle 110of FIG. 5, e.g., the ventricular event is in the range of approximately150 BPM to 190 BPM in this example. Because, as described above, aventricular tachycardia in this range may escape detection using thescheme set forth in FIG. 5, the VA interval is restarted with the VTboundary interval. (Block 130). As mentioned earlier, this actionessentially moves the VA curve 104A upwardly to the VT boundary rateinterval. This action has the effect of slowing the pacing rate, asevidence by the similarly displaced AA interval curve 100A, so thatatrial pacing events are precluded until the ventricular tachycardia maybe sensed and treated.

One advantage of this approach is that it prevents atrial pacing fromobscuring the detection of ventricular tachycardia without theconstraints of limiting the cardiac stimulator's programmable parameterranges. Furthermore, the decision set forth in Block 124 offers theadvantage of applying tachycardia hysteresis only when the ventricularactivity indicates a potential ventricular tachycardia, so thattachycardia hysteresis is not applied to slower ventricular events whichwould effectively reduce the MPR. Also, the decision set forth in Block128 ensures that on cycles with a very short AV interval and a resultinglong operational VA interval (longer than the VT interval), the MPR willnot be exceeded. Finally, the restarting process set forth in Block 130provides a mechanism for tachyarrhythmia hysteresis that allowsventricular tachyarrhythmia detection by extending the pacing rate.

While the technique described with respect to FIGS. 6 and 7 clearlyoffers many advantages, it should be understood that the technique maybe altered in various ways. For example, as mentioned much earlier withrespect to FIG. 3, the cardiac stimulator 10 may be programed withmultiple rate boundaries that define a plurality of differenttachyarrhythmia ranges. For example, as illustrated in FIG. 3, theTACH-1 range defines a range in which tachyarrhythmias may be welltolerated by the patient. In such a circumstance, the techniquedescribed in reference to FIGS. 6 and 7 may be modified to replace theVT rate detection boundary with the boundary between the TACH-1 andTACH-2 ranges, which in this example may be 175 BPM. By referring toFIG. 8, it can be seen by references to curves 100B and 104B that thisaction causes less fluctuation in the MPR in the portion of the graph tothe right of the point 106 as compared with the technique described withreference to FIGS. 6 and 7. Disadvantageously, however, it should alsobe noted that there exists a region between about 150 BPM and about 175BPM, as illustrated by the triangle 110A, where an atrial pace eventcould obscure a ventricular tachyarrhythmia However, as statedpreviously, if ventricular tachyarrhythmias in this range are welltolerated by the patient, the fact that some of these ventricular eventsremain undetected should not pose any problems for the patient, whileallowing the cardiac stimulator 10 to operate in a more physiologicallycorrect manner.

In the techniques described in reference to FIGS. 6-8, it should benoted that the VA interval curve 104A, 104B remains above the VTinterval curve 108 throughout most of the region of interest. Becausethe lengthening of the VA interval lengthens the AA interval, and thusreduces the MAR, it may be desirable to use a technique which sets theVA interval curve 104 at or slightly above the VT interval curve 108 andallows the VA interval curve 104 to follow the VT interval curve 108. Atechnique of this type allows the MPR to increase steadily back to itsnormal level as the VT interval shortens.

An example of this type of technique is illustrated in FIGS. 9 and 10.It should be noted that identical or similar reference numerals and thesame MPR and tachycardia rate detection boundary are used in FIG. 9 asin the previous FIGS. 5 and 6. In particular, it should be noted thatthe AV interval curve 102 and the VT interval curve 108 are the same inthis example as in the example illustrated in FIGS. 5 and 6. However, itshould be noted that the VA interval curve 104C is skewed upwardly atabout the VT rate detection boundary of 150 BPM, as illustrated by thepoint 105B. Indeed, as illustrated by the VA interval curve 104C in FIG.9, the VA interval is lengthened at about the VT rate detection boundaryto make it equal to or greater than the longest VT interval illustratedby the VT interval curve 108. Due to the additive effects of the AVinterval curve 102 and the VA interval curve 104C, this actioneffectively increases the AA interval at point 107B, and thus reducesthe atrial pacing rate, slightly in the presence of high rateventricular activity. Thus, it should be noted that the AA intervalcurve 100C skews upwardly in a manner similar to that of the VA intervalcurve 104C. It should also be noted that this action removes thetriangle 110. As the ventricular activity rises from about 150 BPMthrough about 190 BPM, the VA curve 104C and the AA curve 100C follow asimilar downward slope until they drop back to previous levels at points109B and 111B, respectively.

Referring additionally to FIG. 10, when any ventricular event isdetected at or above the VT rate detection boundary, the VA interval isrestarted with the larger of the VT boundary interval or the operationalVA delay. The operational VA delay is defined as the desired AA intervalminus the actual proceeding AV interval. In a specific exampleillustrated in the flow chart 140, when a ventricular event at or abovethe VT rate detection boundary is detected, the operational VA delay iscomputed (Block 142). It is then determined whether the time from thelast ventricular event, i.e., the VV interval, is less than or equal tothe VT boundary interval. (Block 144). If the VV interval is less thanor equal to the VT rate detection boundary, the detected ventricularevent is not a ventricular tachycardia Therefore, the cardiac stimulatorcontinues to operate in the region of the graph to the left of the MPR106. Accordingly, the VA interval is restarted with the operational VAdelay as illustrated in both FIGS. 5 and 9. (Block 146).

However, if the VV interval is greater than the VT rate detectionboundary, then the ventricular event is indicative of a ventriculartachyarrhythmia. Thus, the cardiac stimulator begins to operate in theregion of the graph of FIG. 9 to the right of the MPR 106. Thus, the VAinterval is restarted with the VT boundary interval and the VA intervalis extended so that the AA interval does not exceed the MPR. (Block148). As mentioned earlier, this action essentially moves the VAinterval curve 104C upwardly to the VT boundary rate interval and causesit to follow the VT interval curve 108. This action has the effect ofslowing the pacing rate, as evidence by the similarly displaced AAinterval curve 100C, so that atrial pacing events are precluded untilthe ventricular tachycardia maybe sensed and treated. It should also benoted that another ventricular tachycardia rate boundary, such as theTACH-1/TACH-2 boundary, may be substituted for the VT boundary rateinterval in this technique in much the same manner as described in FIG.8.

Although the techniques described above with reference to FIGS. 6-10involve curve shifting which induces tachycardia hysteresis, variousother actions may be taken alone, or in combination, to improve theability of a cardiac stimulator to detect ventricular tachyarrhythmiaswhich might otherwise be obscured by an atrial pacing event. Asdiscussed previously, the cardiac stimulator 10 is advantageouslyprogrammable. Thus, the programmable ranges of various parameters may berestricted to reduce or eliminate the circumstance in which atrialpacing obscures ventricular tachyarrhythmias. For example, the VT ratedetection boundary may be set higher than the intersection of the VTinterval curve 108 and the VA interval curve 104. Thus, in this example,the VT rate detection boundary would be set at about 190 BPM. Althoughthis action may be suitable for certain patients that can tolerateventricular tachyarrhythmias in the range below 190 BPM, such actionwould typically not fit the needs of most patients. Of course, asillustrated in FIG. 11, the VT rate detection boundary may be set at anintermediate point such as the intersection between the TACH-1 range andthe TACH-2, range in instances where a patient may tolerate a certainrange of ventricular tachyarrhythmia rather well. OF course, it shouldbe understood that such action only has the effect of decreasing thesize of the region, illustrated by the triangle 110B, where ventriculartachyarrhythmia may be obscured by atrial pacing, but it does so at theexpense of disabling the cardiac stimulator from detecting anyventricular tachyarrhythmias up to the TACH-2 boundary.

As illustrated in FIG. 12, the MPR may be set low enough so that theresulting VA interval curve 104D is raised above the VT interval curve108 in the region above the VT rate detection boundary. However, it canbe seen that this action may significantly limit the MPR 106. Forinstance, as illustrated in this example by the AA interval curve 100D,the MPR must be limited to approximately 110 BPM in order to raise theVA interval curve 104D above the VT interval curve 108 in the regionabove the VT rate detection boundary.

As another example, the AV interval curve 102A may be reduced so thatthe resulting VA interval curve 104E is raised above the VT intervalcurve 108 in the region above the VT rate detection boundary, asillustrated in FIG. 13. This action has the effect of retaining thedesired VT rate detection boundary and the desired MPR However, theshortened AV interval may cause problems such as inadequate ventricularfilling. Of course, the three techniques described in FIGS. 11, 12, and13 may be used in selected combinations to program the cardiacstimulator 10 to best fit a particular patient's needs while minimizingthe range in which ventricular tachyarrhythmias may be obscured by anatrial pacing event.

The techniques described above are advantageously embodied as softwareroutines and/or programing limits that are resident in the memory 36 ofthe cardiac stimulator 10 and executed by the microprocessor 32. Suchroutines may be programmed into the cardiac stimulator 10 at the time ofmanufacturing, or they may be loaded afterward via the programmer 35. Ofcourse, these techniques could also be implemented by an appropriatestate machine or other suitable hardware, or by a combination ofhardware and software.

While the invention may be susceptible to various modifications andalternative forms, specific embodiments have been shown by way ofexample in the drawings and have been described in detail herein.However, it should be understood that the invention is not intended tobe limited to the particular forms disclosed. Rather, the invention isto cover all modifications, equivalents, and alternatives falling withinthe spirit and scope of the invention as defined by the followingappended claims.

What is claimed is:
 1. A cardiac stimulator comprising: a ventricularcircuit adapted to deliver a ventricular signal indicative of aventricular event; an atrial circuit adapted to deliver an atrial signalindicative of an atrial event and adapted to deliver electricalstimulation to the atrium of the heart; and a control circuit executingan algorithm for controlling the cardiac stirnulator, the controlcircuit being coupled to the atrial circuit and to the ventricularcircuit to receive the atrial and ventricular signals, the algorithm:determining an interval between successive ventricular events, referredto as a VV interval, determining an operational VA delay by subtractingan AV interval from an AA interval, determining whether the VV intervalis less than a ventricular tachyarrhythmia boundary interval, if the VVinterval is less than the boundary interval, restarting a VA intervalwith the operational VA delay, if the VV interval is not less than theboundary interval, determining whether the operational VA delay is lessthan the boundary interval, restarting the VA interval with theoperational VA delay in response to the operational VA delay not beingless than the boundary interval, and restarting the VA interval with theboundary interval in response to the operational VA delay being lessthan the boundary interval.
 2. The cardiac stimulator, as set forth inclaim 1, wherein the boundary interval defines an interval betweennormal sinus rate and a ventricular tachyarrhythmia.
 3. The cardiacstimulator, as set forth in claim 1, wherein the boundary intervaldefines an interval between a well-tolerated ventricular tachyarrhythmiaand a moderately-tolerated ventricular tachyarrhythmia.
 4. A method ofoperating a cardiac stimulator comprising the acts of: determining anoperational VA delay by subtracting an AV interval from an AA interval,deterring whether a VV interval is less than a ventriculartachyarrhythmia boundary interval, if the VV interval is not less thanthe boundary interval, restarting a VA interval with the operational VAdelay, if the VV interval is less than the boundary interval,determining whether the operational VA delay is less than the boundaryinterval, restarting the VA interval with the operational VA delay inresponse to the operational VA delay not being less than the boundaryrate interval, and restarting the VA interval with the boundary intervalin response to the operational VA delay being less than the boundaryinterval.
 5. The method, as set forth in claim 4, wherein the boundaryinterval defines an interval between normal sinus rate and a ventriculartachyarrhythmia.
 6. The method, as set forth in claim 4, wherein theboundary interval defines an interval between a well-toleratedventricular tachyarrhythmia and a moderately-tolerated ventriculartachyarrhythmia.
 7. A method of operating a cardiac stimulatorcomprising the acts of: determining an operational VA delay bysubtracting an AV interval from an AA interval, determining whether a Winterval is less than a ventricular tachyarrhythmia boundary interval,if the VV interval is not less than the boundary interval, restarting aVA interval with the operational VA delay, and if the VV interval isless than the boundary interval, restarting the VA interval with theboundary interval.
 8. The method, as set forth in claim 7, wherein theboundary interval defines an interval between normal sinus rate and aventricular tachyarrhythmia.
 9. The method, as set forth in claim 7,wherein the boundary interval defines an interval between awell-tolerated ventricular tachyarrhythmia and a moderately-toleratedventricular tachyarrhythmia.
 10. A cardiac stimulator comprising: acontrol circuit including: computational circuitry adapted to determinean operational VA delay by subtracting an AV interval from an AAinterval; detection circuitry adapted to determine whether a ventriculartachyarrhythmia is present; and timing circuitry adapted to time a VAinterval determined based on whether the ventricular tachyarrhythmia ispresent and at least one of the operational VA delay and a predeterminedventricular tachyarrhythmia rate boundary interval; and an atrialstimulus generator adapted to deliver a pace at the end of the VAinterval.
 11. The cardiac stimulator, as set forth in claim 10, whereinthe timing circuitry includes a timer with restart circuitry, andwherein the VA interval is set to the ventricular tachyarrhythmia rateboundary interval if the ventricular tachyarrhythmia is present and theoperational VA delay is less than the ventricular tachyarrhythmia rateboundary interval.
 12. The cardiac stimulator, as set forth in claim 11,wherein the VA interval is set to the operational VA delay if theventricular tachyarrhythmia is present and the operational VA delay isnot less than the ventricular tachyarrhythmia rate boundary interval.13. The cardiac stimulator, as set forth in claim 12, wherein the VAinterval is set to the operational VA delay if the ventriculartachyarrhythmia is not present.
 14. The cardiac stimulator, as set forthin claim 13, wherein the detection circuitry includes a comparatorhaving a first input representative of a VV interval, a second inputrepresentative of the ventricular tachyarrhythmia rate boundaryinterval, and an output representative of whether the ventriculartachyarrhythmia is present.
 15. The cardiac stimulator, as set forth inclaim 10, wherein the timing circuitry includes a timer with restartcircuitry, and wherein the VA interval is set to the ventriculartachyarrhythmia rate boundary interval, if the ventriculartachyarrhythmia is present.
 16. The cardiac stimulator, as set forth inclaim 15, wherein the VA interval is set to the operational VA delay ifthe ventricular tachyarrhythmia is not present.
 17. The cardiacstimulator, as set forth in claim 16, wherein the detection circuitryincludes a comparator having a first input representative of a VVinterval, a second input representative of the ventriculartachyarrhythmia rate boundary interval, and an output representative ofwhether the ventricular tachyarrhythmia is present.
 18. A method ofoperating a cardiac stimulator, the method comprising: determining anoperational VA delay by subtracting an AV interval from an AA interval;detecting a ventricular tachyarrhythmia; determining a VA interval basedon whether the ventricular tachyarrhythmia is present and at least oneof the operational VA delay and a predetermined ventriculartachyarrhythmia rate boundary interval; and delivering a pace at the endof the VA interval.
 19. The method, as set forth in claim 18, whereindetermining the VA interval includes setting the VA interval to theventricular tachyarrhythmia rate boundary interval if the ventriculartachyarrhythmia is detected and the operational VA delay is less thanthe ventricular tachyarrhythmia rate boundary interval.
 20. The method,as set forth in claim 19, wherein determining the VA interval furtherincludes setting the VA interval to the operational VA delay if theventricular tachyarrhythmia is detected and the operational VA delay isnot less than the ventricular tachyarrhythmia rate boundary interval.21. The method, as set forth in claim 20, wherein determining the VAinterval further includes setting the VA interval to the operational VAdelay if the ventricular tachyarrhythmia is not detected.
 22. Themethod, as set forth in claim 21, wherein the predetermined ventriculartachyarrhythmia rate boundary interval is a predetermined VV intervalcorresponding to one of: a first boundary between a normal sinus rateand a ventricular tachyarrhythmia rate; and a second boundary between awell-tolerated ventricular tachyarrhythmia rate and amoderately-tolerated ventricular tachyarrhythmia rate.
 23. The method,as set forth in claim 22, wherein detecting the ventriculartachyarrhythmia includes: comparing a VV interval to the ventriculartachyarrhythmia rate boundary interval; and declaring a ventriculartachyarrhythmia if the VV interval is less than the ventriculartachyarrhythmia rate boundary interval.
 24. The method, as set forth inclaim 18, wherein determining the VA interval includes setting the VAinterval to the ventricular tachyarrhythmia rate boundary interval ifthe ventricular tachyarrhythmia is detected.
 25. The method, as setforth in claim 24, wherein determining the VA interval includes settingthe VA interval to the operational VA delay if the ventriculartachyarrhythmia is not detected.
 26. The method, as set forth in claim25, wherein the predetermined ventricular tachyarrhythmia rate boundaryinterval is a predetermined VV interval corresponding to one of: a firstboundary between a normal sinus rate and a ventricular tachyarrhythmiarate; and a second boundary between a well-tolerated ventriculartachyarrhythmia rate and a moderately-tolerated ventriculartachyarrhythmia rate.
 27. The method, as set forth in claim 26, whereindetecting the ventricular tachyarrhythmia includes: comparing a VVinterval to the ventricular tachyarrhythmia rate boundary interval; anddeclaring a ventricular tachyarrhythmia if the VV interval is less thanthe ventricular tachyarrhythmia rate boundary interval.